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Allelotyping of Butadiene-Induced Lung and Mammary Adenocarcinomas of B6C3F1 Mice: Frequent Losses of Heterozygosity in Regions Homologous to Human Tumor-Suppressor Genes

To identify the potential involvement of tumor-suppressor gene inactivation during neoplastic development in B6C3F1 mice, genetic losses were determined from allelotypes of butadiene-induced lung and mammary adenocarcinomas. By using length polymorphisms in restriction fragments and simple sequence... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America 26 April 1994, Vol.91(9), pp.3759-3763
Main Author: Wiseman, Roger W.
Other Authors: Cochran, Charles , Dietrich, William , Lander, Eric S. , Soderkvist, Peter
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 00278424
Link: https://www.jstor.org/stable/2364530
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recordid: jstor_archive_232364530
title: Allelotyping of Butadiene-Induced Lung and Mammary Adenocarcinomas of B6C3F1 Mice: Frequent Losses of Heterozygosity in Regions Homologous to Human Tumor-Suppressor Genes
format: Article
creator:
  • Wiseman, Roger W.
  • Cochran, Charles
  • Dietrich, William
  • Lander, Eric S.
  • Soderkvist, Peter
subjects:
  • Health sciences -- Medical conditions -- Diseases
  • Biological sciences -- Biology -- Genetics
  • Biological sciences -- Biology -- Cytology
  • Biological sciences -- Biology -- Anatomy
  • Biological sciences -- Biology -- Genetics
  • Biological sciences -- Biology -- Genetics
  • Biological sciences -- Biology -- Genetics
  • Applied sciences -- Laboratory techniques -- Nucleic acid amplification techniques
  • Health sciences -- Medical conditions -- Diseases
  • Biological sciences -- Biology -- Genetics
ispartof: Proceedings of the National Academy of Sciences of the United States of America, 26 April 1994, Vol.91(9), pp.3759-3763
description: To identify the potential involvement of tumor-suppressor gene inactivation during neoplastic development in B6C3F1 mice, genetic losses were determined from allelotypes of butadiene-induced lung and mammary adenocarcinomas. By using length polymorphisms in restriction fragments and simple sequence repeats, or "microsatellites," markers on each autosome were analyzed for allele losses in tumor DNAs. Losses of heterozygosity on chromosome 11 were observed at several loci surrounding the p53 tumor-suppressor gene (Trp53) in 12 of 17 mammary tumors and 2 of 8 lung tumors. Although most of these alterations appeared to result from nondisjunction, at least two examples of somatic recombination or deletion were also observed. Southern analysis revealed a homozygous deletion of the remaining Trp53 allele of one of these mammary tumors. Losses of heterozygosity were also detected at the Rb-1 tumor-suppressor gene in 7 of 17 mammary tumors and 1 lung tumor. Finally, frequent allele losses were observed on chromosome 4 in lung tumors. Analysis of nine chromosome 4 loci defined an interstitial deletion containing the Ifa gene cluster in one of the lung tumors. A tumor-suppressor gene was previously mapped to this region of chromosome 4 in studies with somatic cell hybrids. In addition, homozygous deletions have been reported in a homologous region of human chromosome 9p for acute lymphocytic leukemias, glioblastomas, melanomas, and lung carcinomas. These findings suggest that the inactivation of tumor-suppressor genes including Trp53, Rb-1, and an unidentified gene on chromosome 4 plays a significant role during carcinogenesis in mice.
language: eng
source:
identifier: ISSN: 00278424
fulltext: fulltext
issn:
  • 0027-8424
  • 00278424
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titleAllelotyping of Butadiene-Induced Lung and Mammary Adenocarcinomas of B6C3F1 Mice: Frequent Losses of Heterozygosity in Regions Homologous to Human Tumor-Suppressor Genes
creatorWiseman, Roger W. ; Cochran, Charles ; Dietrich, William ; Lander, Eric S. ; Soderkvist, Peter
ispartofProceedings of the National Academy of Sciences of the United States of America, 26 April 1994, Vol.91(9), pp.3759-3763
identifierISSN: 00278424
subjectHealth sciences -- Medical conditions -- Diseases ; Biological sciences -- Biology -- Genetics ; Biological sciences -- Biology -- Cytology ; Biological sciences -- Biology -- Anatomy ; Biological sciences -- Biology -- Genetics ; Biological sciences -- Biology -- Genetics ; Biological sciences -- Biology -- Genetics ; Applied sciences -- Laboratory techniques -- Nucleic acid amplification techniques ; Health sciences -- Medical conditions -- Diseases ; Biological sciences -- Biology -- Genetics
descriptionTo identify the potential involvement of tumor-suppressor gene inactivation during neoplastic development in B6C3F1 mice, genetic losses were determined from allelotypes of butadiene-induced lung and mammary adenocarcinomas. By using length polymorphisms in restriction fragments and simple sequence repeats, or "microsatellites," markers on each autosome were analyzed for allele losses in tumor DNAs. Losses of heterozygosity on chromosome 11 were observed at several loci surrounding the p53 tumor-suppressor gene (Trp53) in 12 of 17 mammary tumors and 2 of 8 lung tumors. Although most of these alterations appeared to result from nondisjunction, at least two examples of somatic recombination or deletion were also observed. Southern analysis revealed a homozygous deletion of the remaining Trp53 allele of one of these mammary tumors. Losses of heterozygosity were also detected at the Rb-1 tumor-suppressor gene in 7 of 17 mammary tumors and 1 lung tumor. Finally, frequent allele losses were observed on chromosome 4 in lung tumors. Analysis of nine chromosome 4 loci defined an interstitial deletion containing the Ifa gene cluster in one of the lung tumors. A tumor-suppressor gene was previously mapped to this region of chromosome 4 in studies with somatic cell hybrids. In addition, homozygous deletions have been reported in a homologous region of human chromosome 9p for acute lymphocytic leukemias, glioblastomas, melanomas, and lung carcinomas. These findings suggest that the inactivation of tumor-suppressor genes including Trp53, Rb-1, and an unidentified gene on chromosome 4 plays a significant role during carcinogenesis in mice.
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titleAllelotyping of Butadiene-Induced Lung and Mammary Adenocarcinomas of B6C3F1 Mice: Frequent Losses of Heterozygosity in Regions Homologous to Human Tumor-Suppressor Genes
descriptionTo identify the potential involvement of tumor-suppressor gene inactivation during neoplastic development in B6C3F1 mice, genetic losses were determined from allelotypes of butadiene-induced lung and mammary adenocarcinomas. By using length polymorphisms in restriction fragments and simple sequence repeats, or "microsatellites," markers on each autosome were analyzed for allele losses in tumor DNAs. Losses of heterozygosity on chromosome 11 were observed at several loci surrounding the p53 tumor-suppressor gene (Trp53) in 12 of 17 mammary tumors and 2 of 8 lung tumors. Although most of these alterations appeared to result from nondisjunction, at least two examples of somatic recombination or deletion were also observed. Southern analysis revealed a homozygous deletion of the remaining Trp53 allele of one of these mammary tumors. Losses of heterozygosity were also detected at the Rb-1 tumor-suppressor gene in 7 of 17 mammary tumors and 1 lung tumor. Finally, frequent allele losses were observed on chromosome 4 in lung tumors. Analysis of nine chromosome 4 loci defined an interstitial deletion containing the Ifa gene cluster in one of the lung tumors. A tumor-suppressor gene was previously mapped to this region of chromosome 4 in studies with somatic cell hybrids. In addition, homozygous deletions have been reported in a homologous region of human chromosome 9p for acute lymphocytic leukemias, glioblastomas, melanomas, and lung carcinomas. These findings suggest that the inactivation of tumor-suppressor genes including Trp53, Rb-1, and an unidentified gene on chromosome 4 plays a significant role during carcinogenesis in mice.
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titleAllelotyping of Butadiene-Induced Lung and Mammary Adenocarcinomas of B6C3F1 Mice: Frequent Losses of Heterozygosity in Regions Homologous to Human Tumor-Suppressor Genes
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abstractTo identify the potential involvement of tumor-suppressor gene inactivation during neoplastic development in B6C3F1 mice, genetic losses were determined from allelotypes of butadiene-induced lung and mammary adenocarcinomas. By using length polymorphisms in restriction fragments and simple sequence repeats, or "microsatellites," markers on each autosome were analyzed for allele losses in tumor DNAs. Losses of heterozygosity on chromosome 11 were observed at several loci surrounding the p53 tumor-suppressor gene (Trp53) in 12 of 17 mammary tumors and 2 of 8 lung tumors. Although most of these alterations appeared to result from nondisjunction, at least two examples of somatic recombination or deletion were also observed. Southern analysis revealed a homozygous deletion of the remaining Trp53 allele of one of these mammary tumors. Losses of heterozygosity were also detected at the Rb-1 tumor-suppressor gene in 7 of 17 mammary tumors and 1 lung tumor. Finally, frequent allele losses were observed on chromosome 4 in lung tumors. Analysis of nine chromosome 4 loci defined an interstitial deletion containing the Ifa gene cluster in one of the lung tumors. A tumor-suppressor gene was previously mapped to this region of chromosome 4 in studies with somatic cell hybrids. In addition, homozygous deletions have been reported in a homologous region of human chromosome 9p for acute lymphocytic leukemias, glioblastomas, melanomas, and lung carcinomas. These findings suggest that the inactivation of tumor-suppressor genes including Trp53, Rb-1, and an unidentified gene on chromosome 4 plays a significant role during carcinogenesis in mice.
pubNational Academy of Sciences of the United States of America
doi10.1073/pnas.91.9.3759
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date1994-04-26